Some humans are believed to collapse part of their upper airway as they inspire during sleep causing increased resistance to airflow resulting in disruption of physiologic sleep.
Obstructive Sleep Apnea (OSA) is the term applied to this phenomenon, and it is diagnosed using electroencephalography (EEG), electro-oculography (EOG), electromyography (EMG), electrocardiography (ECG), and pulse oximetry (POX)—all well-established diagnostic tools. Breathing effort is measured as expansion of the chest and abdomen by recording the stretch of belts fitted to subjects during the study. Airflow is measured at the nose and mouth by a variety of sensors. Measurements of airflow and respiratory effort are central to the understanding of respiratory dynamics of sleep, yet these measurements are the least reliable of those available.
Inspiration in a healthy adult human creates a trans-thoracic pressure gradient of about 10 cm water by changing the position of the diaphragm and chest wall, thus expanding the chest volume and reducing intra-thoracic air pressure relative to ambient atmospheric pressure. The reduced intra-thoracic pressure causes air to flow into the lungs to equilibrate the pressure. At the same time, airway resistance in the lungs is decreasing because the lung is expanding. The inspiratory airflow in the trachea is less than about 0.5 L/sec during sleep, and the pressure gradient is dissipated linearly over about 15 cm of the trachea. As used herein, the term “healthy adult human” is a person who presents an absence of any respiratory failure, i.e. who does not have any clinically significant breathing abnormalities, such as emphysema, asthma, bronchiectasis, chronic bronchitis, and the like or is a person who is massively obese, or has unusual body habitus or has anatomical craniofacial abnormalities, or has had a stroke with bulbar palsy, or has trauma, or any other pathologies that create high, fixed upper airway resistance during sleep.
In a person afflicted with sleep apnea, in contrast, airway resistance increases during inspiration because of a presumed obstruction at the level of the hypo-pharynx (OSA). The trans-thoracic pressure gradient thus created is greater (as much as minus 40 cm water has been measured with an esophageal catheter during polysomnography) as the diaphragm and chest wall muscles contract in an attempt to overcome the increased airway resistance and maintain air flow. There is a theoretical point at which the trans-thoracic pressure gradient will be insufficient to overcome rising airway resistance. At this point, airflow will stop even in the absence of anatomic obstruction.
The act of breathing involves a variable number of inspirations per unit of time (respiratory rate) and a variable volume of air taken into the lungs with each breath (tidal volume). The product of these two is termed the ‘minute ventilation.’ The minute ventilation, or VE, is the amount of inspired air per minute, and is controlled by the amount of dissolved carbon dioxide in the blood. Carbon dioxide (CO2) is a product of combustion of hydrocarbons and is expired from the body in its gaseous form via the lungs. A rising level of dissolved carbon dioxide in the blood causes an increase in minute ventilation sufficient to return the level to normal (40 mmHg). Conversely, a falling level of dissolved carbon dioxide in the blood causes a decrease in minute ventilation sufficient to return the level to normal (40 mmHg). Each person has his/her individual “normal” blood CO2 level which, for adult humans in health, is in a range of about 38 to about 42 mm Hg, wherein mm Hg is the partial pressure of CO2 (pCO2) in a blood sample. During the wakeful state, adjustments in response to rising and falling carbon dioxide levels are made quickly without conscious awareness.
Another form of apnea has been termed ‘central sleep apnea (CSA).’ It has been distinguished from OSA by the absence of apparent respiratory effort. When respiratory effort stops, minute ventilation falls to zero and carbon dioxide begins to accumulate in the blood and cerebrospinal fluid. When the CO2 level exceeds 40 mmHg, inspiration begins again, and this generally causes disturbance of sleep. If, during sleep, the carbon dioxide levels fall low enough, true apnea (TA) will occur. The blood carbon dioxide level during OSA is not known with certainty. Even though respiratory effort is seen and measured in OSA, minute ventilation is presumed to be inadequate (hypoventilation) to maintain normal levels of carbon dioxide in the blood. If that were the case, carbon dioxide would accumulate in the blood and cerebrospinal fluid. During normal, awake respiration (ventilation), changes in blood carbon dioxide are rapidly corrected, but correction is slower in the cerebrospinal fluid. Carbon dioxide is freely diffusible throughout the body, but bicarbonate is transferred slowly across the blood-brain barrier. Bicarbonate neutralizes carbon dioxide that is dissolved in water (carbonic acid) and helps to adjust variations in dissolved carbon dioxide. With slower flux of bicarbonate in the cerebrospinal fluid, corrections in carbon dioxide levels will be slower and synchrony of blood chemistry and breathing dynamics will be impaired.
At sleep onset in health, minute ventilation decreases and arterial carbon dioxide accumulates establishing new parameters for adequacy of ventilation. This means that, during sleep, higher levels of carbon dioxide are necessary to stimulate breathing than during wakefulness. Without conscious awareness, hypoventilation is less discernible and carbon dioxide levels continue to increase. When this happens, an arousal occurs that is defined by convention as an increase in frequency and decrease in amplitude of the EEG. Arousals occur at the end of both ‘Central’ and ‘Obstructive’ apneas and appear, behaviorally, to be signs of respiratory distress. They indicate a switch from autonomic parasympathetic to autonomic sympathetic-nervous-system control caused by the release of stimulatory biochemicals called cathecholamines into the blood causing disruption of physiologic sleep and most of the behaviors seen with sleep-disordered breathing.
The Hering-Breuer reflex, is a vagal afferent (sensory) and efferent (motor) loop that responds to increasing chest wall tension and serves to stop and start inspiration. When chest wall tension is minimal (end expiration), vagal afferents fire at minimal frequency. At maximal chest wall tension (end inspiration), vagal afferents fire at maximal frequency. The respiratory center in the brain ends inspiration in response to this high frequency and expiration occurs passively. During ‘apnea’ with high trans-thoracic pressure gradients, the Hering-Breuer reflex is firing maximally.
Thus, the level of carbon dioxide in the blood determines the rate of respiration and the Hering-Breuer reflex determines the depth. Even though the respiratory effort in OSA appears diminished in ‘apnea’ periods, the trans-thoracic pressure gradient is quite high to match the high airway resistance. Only the resultant airflow is low (hypopnea) or zero (apnea). The damping of the waveform signal of the respiratory effort channels (chest and abdomen) only reflect decreased excursion, not effort. Therefore, the Hering-Breuer reflex is probably functioning normally and the ventilatory response to carbon dioxide is probably normal in both CSA and OSA.
The variable response time to ‘apnea’ (10 to 90 seconds) probably reflects the individual's rate of carbon dioxide accumulation and thus may indirectly reflect the amount of true airflow. For example, a subject who is ‘apneic’ for an extended period of time is probably breathing more effectively than one who is ‘apneic’ for a shorter period of time. Because of the poor technical quality of airflow and respiratory effort measurements, ‘apnea’ and ‘hypopnea’ are largely subjective terms. It may be more accurate to describe OSA as hypoventilation (hypercarbia) during sleep.
Arousals can also occur in the absence of a detectable respiratory event. Less is known about these kinds of arousals, but they may be due to changes in inspiratory air flow that are not detected by available technology. It is likely that all arousals are due to hypercarbia.
OSA is most commonly treated by changing from negative pressure ventilation (increased chest volume, decreased intra-thoracic pressure) to positive pressure ventilation (increased chest volume, increased intra-thoracic pressure). Compressed air is applied at the nose via a tight-fitting mask. The native respiratory rate remains intact, but the ambient air pressure is supra-atmospheric throughout inspiration and expiration. This has been termed Continuous Positive Airway Pressure (CPAP). The same pressure differential is ostensibly created in both forms of ventilation, about 10 cm water, but positive pressure seems to maintain airflow against elevated ambient inspiratory resistance better than negative pressure. Put another way, when mean air pressure above and below the putative obstruction is supra-atmospheric, flow is maintained against elevated inspiratory resistance. But, when air pressure above the putative obstruction is atmospheric but sub-atmospheric below the obstruction, flow is reduced or stopped. In fact, for normal ventilation to be perpetuated, there must be some negative pressure created. Thus, in CPAP administration, the intra-thoracic pressure still falls prior to inspiration and thus creates airflow, but the value around which the sinusoid waveform of ventilation varies is supra-atmospheric during CPAP administration.
Positive pressure also unloads the inspiratory respiratory muscles (diaphragm and chest wall muscles). In patients with chronic respiratory failure, the work of breathing must be quite high to overcome the lowered mechanical advantage and architectural changes of chronic lung disease. Positive pressure ventilation is thought to “rest” these muscles during hours of sleep. This benefit seems unrelated to OSA.
“Tracheotomy” refers to creating a passage between the outside of a patient's body and the inside of his/her windpipe or trachea. There is very little tissue between the skin and the trachea and few blood vessels and nerves at a point low in the front of the neck. An opening can be made safely at this location of the neck, and such procedures have been performed since very early in the history of medicine. “Tracheostomy” refers to creating a useful conduit out of the above referenced opening by inserting a metal or plastic device to maintain the opening and to permit the connection of other devices, such as a mechanical ventilator. Surgical tracheotomy is also an effective empirical treatment for OSA, but it was not developed for that purpose.
Tracheotomy and tracheostomy were developed for critically-ill, hospitalized patients who require mechanical ventilation for prolonged periods of time, such as more than a week. Tracheostomy appliances were designed to replace the use of endotracheal tubes inserted through the nose or mouth of the patient since long-term use of endotracheal tubes can cause unacceptable trauma to the airway and prevents the patient from eating and talking. Typically, the size of tracheostomy openings has been relatively large to permit suctioning and connections to ventilator tubing.
The surgical techniques, devices and management of tracheotomy are applied to patients with profound respiratory failure who require mechanically-assisted ventilation. Tracheotomy provides access for this ventilation. Surgical tracheotomy is also used as an alternate airway when trauma or disease has deprived a patient of the normal upper airway structures. In that case, tracheotomy may be used with or without mechanically-assisted ventilation.
Tracheostomy has been used to treat Obstructive Sleep Apnea Syndrome. In fact, it is the most effective treatment of this disorder. As discussed, supra, Obstructive Sleep Apnea Syndrome occurs when the throat or pharynx increases resistance to air inflow to the trachea during sleep. The location of the anatomical structure causing the resistance is well above the trachea. Thus, an opening created in the trachea permits air to enter the lungs in the event the above referenced resistance occurs in the throat or pharynx.
Examples of tracheostomy appliances are disclosed, for instance, in U.S. Pat. Nos. 5,464,011 issued to Bridge; 4,538,607 issued to Saul; 4,582,058 issued to Depel et al.; 6,193,751 issued to Singer; 4,877,025 issued to Hanson; 3,137,299 issued to Tabor; 3,263,684 issued to Bolton; 4,759,356 issued to Muir; 5,048,518 issued to Eliachar et al.; 5,259,378 issued to Huchon et al.; 5,392,775 issued to Adkins, Jr. et al.; 5,505,198 issued to Siebens et al.; 6,189,534 B1 issued to Zowtiak et al.; and 6,588,428 B2 issued to Shikani et al., and U.S. Patent Application Publication No. 2004/0123868 A1 of Rutter.
While the above referenced tracheostomy appliances may function in an acceptable manner for their intended purposes, there is a need for tracheostomy appliances and methods specifically designed to treat Sleep Apnea Syndromes in adult patients in health.